Abstract

Diabet ic neuropathy is a classical diabetes-specific chronic complication, its prevalence is estimated as 28−55% among all individuals with diabetes in dif ferent sur veys. Two major groups of diabetic neuropathy are generalized symmetrical polyneuropathies and focal and multifocal neuropathies. The former group comprises acute sensory, chronic sensorimotor and autonomic neuropathy and the latter group comprises cranial and focal limb neuropathies, thoracolumbar radiculoneuropathy and proximal motor amyotrophy. Chronic sensorimotor and autonomic neuropathies are the most prevalent forms of diabetic neuropathy. In chronic sensorimotor neuropathy, both small and large nerve fibres can be affected. If the damage of small fibres prevails the patients complain about pain and paresthesias in the feet and occasionally  in the hands with considerable reduction in quality of life. Predominant impairment of large nerve fibres causes numbness, loss of position sense and muscle wasting, which can lead to development of diabetic ulcers and gangrene. The cardiovascular component of autonomic neuropathy can be potentially life-threatening due to silent myocardial infarction or sudden death. The few treatment options interfering with the pathogenesis of neuropathy include thioctic acid and aldose reductase inhibitors, the latter being currently in phase III clinical trials. In symptomatic treatment of neuropathic pain ant idepressants, anticonvulsants and opioids have proved efficacy and a favorable safety profile. However, strict control of serum glucose levels remains the cornerstone of prevention and treatment of diabetic microvascular complications and neuropathy.